摘要
目的 :研究抗癌药斑蝥素对肝癌细胞细胞毒作用的分子机制。方法 :应用基因芯片技术检测 12 .5 μmol/ L 斑蝥素作用于肝癌 QGY770 3细胞 2 4 h后基因表达谱的变化。结果 :斑蝥素抑制细胞表达参与细胞周期进程基因 (如 p 2 7、ref - 1、DN Apolymerase delta、X RCC9等 )、能量代谢基因 (如 malate dehydrogenase、ADP/ ATP translocase等 )、致瘤活性基因 (如 c- myc、tre等 )以及肿瘤特异表达基因 (如 bladder cancer related protein等 )。相反 ,斑蝥素促进了多种细胞生长抑制基因 (如 BCRA2、BTG2、dual- specificity protein phosphatase等 )以及凋亡相关基因 (如 ATL - derived PMA- responsive peptide等 )的表达。 结论 :斑蝥素改变调控细胞周期进程、细胞增殖。
Objective:To study the molecular mechanisms of antitumor agent cantharidin on human cancer cells. Methods:Gene expression profile was identified by cDNA microarrays in hepatic cancer QGY 7703 cells exposed to cantharidin (12.5 μmol/L) for 24 h.Results:Cantharidin treated cells had decreased expression of genes coding for proteins involved in cell cycle progress( p27,DNA polymerase delta,XRCC,ref 1 ),energy metabolism( malate dehydrogenase,ADP/ATP translocase ),oncogenic activation( c myc,tre )and tumor specific expression( bladder cancer related protein ). In contrast,these treated cells overexpressed several genes encoding intracellular growth inhibitory proteins( BCRA2,BTG2,dual specificity protein phosphatase )and proapoptotic genes( ATL derived PMA responsive peptide ).Conclusion:These findings suggest that alterations in specific genes involved in modulating the cell cycle progress,cell proliferation,energy metabolism,and apoptosis cascades may be responsible for cantharidin mediated cytotoxicity.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2003年第6期645-649,共5页
Academic Journal of Second Military Medical University
基金
上海市临床医学中心发展基金 ( ZX0 1B0 5 )
